The effect of taurine and its metabolites on the pathogenic functions of rheumatoid arthritis fibroblast-like synoviocytes

Fibroblast-like synoviocytes (FLS) are thought to contribute to rheumatoid arthritis (RA) pathogenesis via several mechanisms, e.g. by secreting numerous pro-inflammatory cytokines or by COX-2-generated synthesis of prostaglandin E₂ (PGE₂), another pleiotropic mediator of inflammation. Moreover, synovial hyperplasia, the most characteristic feature of RA, is belived to be a consquence of intractable proliferation and partial resistance of FLS to apoptosis. We have previously reported taurine chloramine (Tau-Cl) to represent potent inhibitory compound counteracting in vitro these pathogenic function of RA FLS. Tau-Cl is a chlorinated derivative of a dominant free amino acid taurine (Tau), originates from activated neutrophils, and is further converted into sulphoacetaldehyde (SA). The effect of SA on RA FLS functions has not been estimated yet. Therefore, the aim of present study was to compare simultaneously the effect of Tau, Tau-Cl and SA on select cellular responses of FLS, using FLS isolated from the same RA patients. We have found that among tested compounds only Tau-Cl, but neither Tau nor SA, exerts inhibitory effect on RA FLS proliferation as well as on the synthesis of IL-6 and PGE₂ by these cells.